Therapeutic device and method for treating diseases of cardiac muscle

ABSTRACT

An apparatus and method for conferring a therapeutic current to the heart is provided. The apparatus includes a first electrode, a second electrode, a current generator and a controller. The apparatus may further include a sensor. The sensor is generally configured to measure field strength between the first and second electrode. The sensor may also monitor the cardiac cycle. The method includes applying an electric stimulus to the heart and sensing the electric field generated by the electric stimulus to prevent the level of current from inducing unwanted depolarization.

CROSS-REFERENCE TO RELATED APPLICATIONS

This application is a divisional of continuation-in-part U.S.application Ser. No. 09/756,567, filed Jan. 8, 2001, now U.S. Pat No.6,560,489 which claims priority to a application of U.S. patentapplication Ser. No. 09/638,233, filed Aug. 14, 2000 (now abandoned),which claims priority from U.S. Provisional Application Ser. No.60/143,510, filed Aug. 24, 1999. The above-referenced Patent andProvisional Applications are incorporated by reference in the presentapplication in their entirety.

BACKGROUND OF THE INVENTION

1. Field of the Invention

The present invention relates to an apparatus and method for treatmentof the heart and, more particularly, to an apparatus and method forproviding a therapeutic sub-threshold electrical current to the heart.

2. Discussion of the Related Art

A wide range of therapies is available for the treatment of cardiactissue damage, heart failure and for treatment of the specificunderlying disease processes. Most of these therapies may be classifiedas drugs, surgical intervention, or cardiac assist devices. The cardiacassist devices assist the heart in pumping function to relieve the heartof stresses during the healing process. If a condition is caused bycoronary disease or is exacerbated by conduction defects, availabletherapies include either bypass surgery or angioplasty in the case ofthe former, or pacemaker therapy in the case of the latter. Theabove-mentioned damage and diseases as well as other factors set inmotion the condition known as congestive heart failure (CHF). Althoughtherapies have addressed treating specific indications, few therapiesaddress the problem of tissue remodeling.

Tissue remodeling refers to the histological alteration of tissue overtime. Remodeling may include histological and/or biochemical changes atthe tissue, cellular and molecular levels. Tissue remodeling can beeither beneficial or degenerative to a patient. Tissue remodeling isdegenerative when histologically and/or biochemically normal tissue isaltered in such a way that the tissue no longer functions properly.Degenerative tissue remodeling may occur progressively in patientssuffering from congestive heart failure or atrial fibrillation. In thosepatients, the resulting remodeling adversely affects the heart'sperformance and exacerbates the deteriorating condition of the heart.Tissue remodeling is beneficial when a histologically and/orbiochemically abnormal tissue is reverted to a more normal histologyand/or biochemistry.

Recently, one aspect of degenerative remodeling due to the progressionof CHF has been identified as the breakdown in the collagen of theextra-cellular matrix. The extra-cellular matrix is the externalstructure between the cells in the heart that primarily consists of amatrix of type I collagen and fibrils. This matrix is connected to thecytoskeletal myofibrils within the myocardial cells. The matrix providestensile strength to the tissue, governs the tissue's stiffness, andpreserves the alignment of the myocardial cells. Abnormalities in thematrix's composition and concentration during dilation, hypertrophy andischemic injury inhibit the function of the heart and may lead to heartfailure.

Endogenous factors regulate the breakdown and/or re-establishment ofcollagen and other extra-cellular matrix components. These endogenousfactors are diverse and their functions and structures are the subjectof much research. The endogenous factors include a family of enzymesknown as the matrix metalloproteinases. The matrix metalloproteinasescatalyze a reaction breaking down the extra-cellular matrix. Theenzymatic activity of the matrix metalloproteinases is countered by aset of proteins known as the tissue inhibitors of the matrixmetalloproteinases (TIMPs). The TIMPs inhibit the enzymatic activity ofthe matrix metalloproteinases. The matrix metalloproteinase:TIMP ratiois typically around 1.1:1.0 in a normal heart. The ratio may be around6:1 or 7:1 by the end stage of CHF. Research has shown that theinterruption of matrix metalloproteinases with pharmaceutical agentsreduces chamber dilation in animal models for CHF. Relatedly, thisresearch has shown an overall increase in the collagen content due tothe treatments.

In addition, the inhibition of matrix metalloproteinases and,presumably, the subsequent increase in collagen have been shown toresult in the beneficial remodeling of treated diseased hearts.Interruption of matrix metalloproteinases with drug therapy has beenshown to reduce chamber dilation in CHF animal models. However, drugtherapy for inhibiting matrix metalloproteinases may present potentiallyserious problems. The systemic inhibition of the matrixmetalloproteinases has been found to produce a variety of side effects,such as joint and muscle pain. Therefore, a need exists for a therapythat specifically targets the desired tissue or organ to be treated.

Another aspect of degenerative remodeling is ischemic cardiomyopathy. Inischemic cardiomyopathy, a loss of blood flow or ischemia to a portionof the heart muscle causes not just weakness or scarring to thatportion, but subsequently a progression to chamber dilation and failure.The loss of blood flow may be the result of arteriosclerosis, othercardiac diseases, or injury, which can result in a partial or completeblocking of blood flow to a region of the heart. The limited blood flowmay result in localized tissue death known as an infarction. Thepresence of an infarction weakens contraction in that region andtherefore degrades the heart's performance. To compound the problem, themyocardial tissue adjacent to the infarction typically receives areduced blood flow and, therefore, exhibits reduced contractility. Thezone receiving the reduced blood flow is known as an ischemic zone. Theischemic zone further inhibits the hearts ability to contract. Further,the elevation of matrix metalloproteinases, reduction in TIMPs, andconsequent degradation of collagen may play an additional role inischemic cardiomyopathy. To improve cardiac output in patients withischemic cardiomyopathies, there is a need to re-establish blood flow tothe ischemic zones.

Re-establishing blood flow to the ischemic zone has been shown toimprove cardiac function. Re-establishing blood flow may be accomplishedthrough angiogenesis in which the body generates additional bloodvessels in a particular region. Prior methods for re-establishing bloodflow and rehabilitating the heart frequently involved invasive surgerysuch as bypass surgery or angioplasty. Other methods have used lasers tobore holes through the infarctions and ischemic zones to promote bloodflow. These surgeries are complicated and dangerous. Therefore, a needexists for a safe non-invasive method for re-establishing blood flow.

As alternatives to surgery, various chemical and biological agents havebeen developed that promote angiogenesis. Genetic engineering has playeda significant role in the development of many of these new agents.However, in practice, direct injection of these angiogenic agents failsto specifically target the ischemic zone. Further, injection of geneticmaterial within a vector is a more biologically complex process andfrequently suffers from a low transfection efficiency. In addition, theintroduction of xenobiotics compounds can be dangerous. The compounditself may be toxic, virulent and/or allergenic. Therefore, a needexists for a therapy for promoting angiogenesis that is efficient anddoes not introduce xenobiotics into a patient. In addition, many of thedrugs prescribed for CHF patients are primarily for palliative orsymptomatic relief These drugs typically do not treat the underlyingdisease process of CHF and their use frequently results in serious orprohibitive side effects. Further, the drugs are typically administeredsystemically and therefore, impact the entire body not just the organ ortissue to be treated. Therefore, a need exists for a therapy capable ofpromoting overall remodeling without inducing unwanted side effects.

Atrial fibrillation is another serious condition in which degenerativetissue remodeling also plays a significant role. As in CHF and coronaryischemic disease, early theories on the cause of atrial fibrillationsuggested that its causes may be multi-factorial, but the onset ofdegenerative tissue remodeling exacerbates atrial fibrillation.

The promotion of healing with electric current stimulation has beenrecognized in medicine for many years. Most commonly, electricity isused to promote bone union in fractures that have proven refractory tonormal healing. The devices used have directly applied the current tothe skin over the fracture. Alternatively, other devices use pulsedelectromagnetic fields (PEMF) that do not require direct skin contact topromote healing.

Electrical stimulation of cardiac tissues has also been utilized totreat various conditions of the heart. Pacemakers provide electricalstimulation above the contraction threshold to treat variousarrhythmias. Further, sub-threshold stimulation currents have been usedto extend the cardiac tissue's refractory period in the treatment oftachycardia and to increase contractility in the cardiac muscle.However, sub-threshold stimuli have not been broadly applied to theheart and adjacent blood vessels to promote healing and tissueremodeling.

Providing electric current stimulation of ischemic zones on the hearthas recently been shown to promote angiogenesis and further, electriccurrent stimulation has been shown to increase collagen type Iproduction in cultured cells. However, directly or indirectly applyingelectrical stimulation to the heart can be dangerous. There is a risk ofinducing a depolarization of the cardiac tissue resulting in an unwantedcardiac contraction. Further, there is a risk of inducing alife-threatening arrhythmia. Therefore, a need exists to provide amethod and apparatus that reduces the risks of providing an electricalstimulation to the heart to promote angiogenesis, to increase collagentype I production, to prevent the breakdown or degradation ofextra-cellular matrix proteins, and to promote other aspects ofbeneficial remodeling.

One problem not addressed by prior methods is the inability toaccurately assess the field strength generated in the region of theheart. Significant variation in body types, conductivity profiles andstimulation thresholds exist between patients. A particular stimuluslevel may be safe when applied to one patient, and yet that samestimulus may evoke an unwanted reaction from another patient. Thus, aneed exists for a method and apparatus for measuring the field strengthof a therapeutic current. Another problem is the artifact created by anapplied stimulus, which may disrupt the sensing and activation of animplanted pacing or defibrillation device. The disruption could resultin stimulation at a high-risk portion of the cardiac cycle, or anundesirable or unnecessary defibrillation shock. Thus, a need alsoexists for a method and apparatus that reduce the likelihood fordisruption of an implanted pacing or defibrillation device.

The apparatus and method of the present invention meet the above needsand provide additional improvements and advantages that will be evidentto those skilled in the art upon review of the specification andfigures.

SUMMARY OF THE INVENTION

The apparatus and method use therapeutic current stimulation thatoptimizes safety and therapeutic benefit in treating cardiac tissue. Theapparatus for remodeling a heart includes a first electrode, a secondelectrode, a current generator, and a controller. The apparatus mayfurther include one or more sensors. The sensors being configured tomeasure field strength from the electrodes and may also monitor thecardiac cycle. The sensors may be implanted in or on the heart or theymay be positioned within the esophagus or trachea. The controller isconfigured to regulate the output from the current generator to maintainthe field strength below the heart's depolarization threshold. Thesensors may further monitor the depolarization of the heart and thecontroller may synchronize the therapeutic electrical stimulation fromthe current generator with a cycle of the heart. The controller'ssynchronization may apply the electrical stimulation during therefractory period of the cardiac cycle. Alternatively or in addition,the sensor may monitor the field strength at a location in or near theheart generated between the first electrode and the second electrode.When monitoring field strength, the controller maintains thesub-threshold therapeutic electrical stimulation from the currentgenerator at a level below a stimulation threshold of the heart. Acardiac defibrillator may also be incorporated as an integral part ofthe device. Further, the apparatus may be integral with a cardiacpacemaker. In addition, the apparatus may utilize the pacemaker's ordefibrillator's electrodes implanted within the patient to eliminate theneed for additional implantation surgery.

The method of the present invention provides cardiac therapy. The methodincludes applying a stimulus to the heart and measuring the fieldstrength generated by applying the stimulus to maintain the fieldstrength below the heart's depolarization threshold and/or sensing thecardiac cycle to establish the varying depolarization threshold andapplying a varying stimulus below the threshold for the particularpoints within the cardiac cycle.

The invention provides many advantages. The present invention providesthe heart with a safe therapeutic current to promote healing of diseasedor inflamed tissue. The invention mitigates the concerns relating to theapplication of therapeutic current to the heart, including but notlimited to the concerns of uncontrolled or dangerous current level andthe possible dangerous asynchronous application of current with respectto the cardiac cycle. The apparatus and method allow for long-termtreatment for beneficial remodeling of the heart while minimizing therisk of damaging tissue.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 illustrates an apparatus in accordance with the presentinvention;

FIG. 2 illustrates a block diagram of an embodiment of an apparatus inaccordance with the present invention; and

FIG. 3 illustrates an embodiment of an apparatus in accordance with thepresent invention having an electrode and sensor implanted in the heart.

FIG. 4 illustrates another embodiment of an apparatus in accordance withthe present invention having a first and second electrode implantedwithin the heart through a coronary vein access.

DETAILED DESCRIPTION OF THE INVENTION

The present invention is described generally as a therapy for promotingremodeling of a patient's heart. Those skilled in the art will recognizethe improvements and advantages conferred by the present invention inthe treatment of heart disease and heart failure, the specificetiologies including, but not limited to, ischemic cardiomyopathy,idiopathic dilated cardiomyopathy, other cardiomyopathies, myocarditisand atrial fibrillation.

An apparatus 10 in accordance with the present invention is shown inFIG. 1. Apparatus 10 includes a current generator 12, a first electrode14, a second electrode 16, a sensor 18, and a controller 20. First driveelectrode 14 and second drive electrode 16 are configured to beimplanted in a chamber of the heart or within the coronary vessels, orare configured to be secured on or near the heart. Typically, theelectrodes are connected to current generator 12 by a conductive wire.Current generator 12 is configured to provide a sub-threshold stimulusthrough heart tissue positioned between first electrode 14 and secondelectrode 16. Current generator 12 allows the adjustment of one or moreparameters of the output current. One or more sensors 18 are configuredto sense the electric field strength in or near the heart resulting fromcurrent generator 12. Sensors 18 may also sense the depolarizations ofthe heart. A typical sensor configuration may include a pair ofendocardial sensing electrodes. Sensors 18 may be implantable, such thatthe sensors may be positioned in, on or around the heart, shown in FIG.3. Alternatively, the sensors may be positioned within a patient'sesophagus or trachea. Sensors 18 are in communication with controller20, either directly by wire or through a telemetry link, to conferinformation indicative of the field strength and may also conferinformation regarding the cardiac cycle. Further, sensor 18 and/orelectrodes 14 and 16 may be integral with a cardiac lead attached to aconventional cardiac pacemaker or defibrillator. The cardiacpacemaker/defibrillator will typically house a battery power source andelectronics. Controller 20 is also in communication with currentgenerator 12, either directly by wire or through a telemetry link.Controller 20, shown in FIG. 1, is integral with current generator 12for exemplary purposes only. Controller 20 is configured to adjust atleast one of the parameters of the sub-threshold electrical stimulusoutput from the current generator and/or to switch the current generatoron and off based on input from sensors 18.

The embodiment shown in FIG. 2 includes a sensor 18, an amplifier 26, ananalog to digital (A/D) converter 28, a controller 20, a currentgenerator 12, a first drive electrode 14 and a second drive electrode16. The configuration shown in FIG. 2 permits the amplification anddigital conversion of the analog data sensed by sensor 18. The digitaldata is received and analyzed by controller 20. Controller 20 determinesthe appropriate therapeutic current based on the sensed data and theparticular therapy being implemented. Controller 20 then communicates acontrolling signal to current generator 12. Based on the controllingsignal, current generator 12 applies the appropriate current levels,frequency output and/or timing to first drive electrode 14 and seconddrive electrode 16. Sensor 18 may be secured to an endocardial lead andpositioned in the right ventricle of the heart, or it may be part of acoronary lead or epicardial lead. In such a configuration, implantedsensor 18 senses cardiac cycle and/or field strengths of signalsresulting from the intrinsic electrical activity and therapeuticcurrent, and these signals are provided to controller 20 through thesignal path of amplifier 26 and A/D converter 28. This informationallows controller 20 to maintain the current from current generator 12at safe but efficacious levels.

As illustrated in FIG. 3, first electrode 14 and second electrode 16 maybe configured for placement in a manner similar to implantabledefibrillator electrodes. First electrode 14 utilizes the defibrillationelectrode of a right ventricular endocardial lead. The defibrillationelectrode affords a broad distribution of current. Electrode 16 isintegral with the housing, or ‘can’ of the implanted device, whichhouses the electronics such as the controller 20 and current generator12. The sub-threshold current flow for the invention will thus flow in abroad path from electrode 14 to the implanted can electrode 16, the canbeing typically implanted in the left pectoral region. Thus the septum,left ventricle and left atrium will incur a fairly uniform density inthis embodiment. In FIG. 3, an additional pair of electrodes maycomprise the sensor 18. The sensor is shown on a catheter placed in thecoronary sinus for exemplary purposes.

Alternatively, electrodes 14 and 16 may be positioned on or in the heartso that when a current flows between the electrodes 14 and 16 thecurrent passes through the region of the heart requiring therapy. Forexample, a lead may include a pair of electrodes spaced about 2centimeters apart as shown in FIG. 4. The lead is shown with a rightatrial access, passing through the coronary sinus, with the electrodes14 and 16 positioned so that they are near an ischemic region in theposterior left ventricle, where therapy is required. Only a significantcurrent density would be realized in the required area in thisembodiment.

Therapy using apparatus 10 may utilize a broad range of currents. Theparticular current used may be optimized to preferentially stimulate acell-initiated angiogenic response, to promote collagen type Iproduction and/or to stimulate another aspect of beneficial remodeling.Current generator 12 typically provides drive currents in the range ofmicro-amperes to milliamperes. The drive current may be between 10microamperes to 10 milliamperes although higher or lower drive currentsmay be used. As discussed above, since the field strength resulting fromthe current in or near the heart is assessed, and the drive currentneeded to achieve a given field strength will vary from patient topatient.

Apparatus 10 may utilize either a direct current (DC) or an alternatingcurrent (AC). When AC current is used, a wide range of frequencies maybe utilized with particular frequencies being tailored to particulartherapies. Typically, the sinusoidal frequencies used are between 2 Hzand 200 Hz, although higher sinusoidal frequencies in the range of tensof kilohertz may be utilized. For example, the application of afrequency of around 20 hertz has been shown to be efficacious inincreasing expression of Type 1 collagen, while higher frequencies havebeen shown to be efficacious in promoting angiogenesis. Alternatively,pulsed fields have proven efficacious in promoting angiogenesis. Pulsedwaveforms typically result in higher frequency components. When lowerfrequencies are utilized the control algorithm implemented by controller20 compensates for the lower depolarization thresholds resultant fromthe lower frequencies.

In one embodiment for current application, the therapeutic current isapplied continuously at a constant level below stimulation thresholdwithout regard to the heart's cycle. A field strength is selected thatis below the stimulation threshold of the myocardial tissue. Forexample, using the 20 Hz sinusoidal waveform, a 200 microamperes/cm²current density may provide an electric field strength within the hearttissue of around 80 mV/cm, given typical values for myocardialresistivity.

In another embodiment for current application, the stimulus amplitudemay be dynamically modified with respect to the cardiac cycle.Typically, the current density may be relatively large during therefractory period and drop to a sub-threshold level outside of theheart's refractory period. Thus, the heart's cycle is monitored asdescribed above. Upon detection of a depolarization event, the currentdensity is increased during a predetermined window. At the conclusion ofa window, typically 200 milliseconds, the current is then lowered to apre-determined level below the depolarization threshold of the subjectheart.

It is recognized that substantial current drain may be required for thisinvention relative to conventional implantable devices such aspacemakers and defibrillators. Well known means of transcutaneousre-charging of the implantable battery may be used to support thisinvention. A separate re-chargeable battery may be used, so as to leavethe critical pacing and defibrillator functions independent of currentdrain from this invention.

Sensors 18 may monitor the electric field strength created by currentgenerator 12 and may also monitor the patient's intrinsic heart rhythm.This monitoring facilitates the safe application of the therapeuticcurrent. The sensed field waveform and/or the patient's intrinsiccardiac biopotentials are communicated to controller 20 to regulatecurrent generator 12. Thus, apparatus 10 mitigates the danger ofuncontrolled or dangerous current levels and/or asynchronous applicationof therapeutic current with respect to the cardiac cycle. The followingembodiments for sensor 18 are provided for exemplary purposes. Uponreview of the present disclosure, those skilled in the art willrecognize that a variety of additional sensor configurations may be usedto monitor the depolarization of the heart and/or to measure fieldstrength in accordance with the present invention.

In one embodiment, sensor 18 is a pair of electrodes secured to acardiac lead, as shown in FIG. 3. The lead is connected to a pacemakeror defibrillator lead system. The electrodes are configured to monitorthe field strength generated by current generator 12. To measure thefield strength, the electrodes may be aligned substantially along a lineor axis formed between the two drive electrodes. Typically, the axisconnecting sensors 18 lie within 30 degrees of the drive electrodes'axis. Alternatively, if sensors 18 are at any given known or measuredangle with respect to the drive electrode axis, the maximum magnitude offield strength can be calculated by dividing the measured value by thecosine of this angle. The electrodes of sensor 18 are electricallycoupled to amplifier 26. Amplifier 26 is configured with a bandwidthsuitable to recover the frequency of the therapeutic current beingadministered. The amplified signal is converted to a digital signal bythe A/D converter 28. A/D converter 28 then communicates the signal tocontroller 20. The therapeutic waveform may be recovered and separatedfrom any noise and biopotentials in the signal using synchronousdemodulation or other techniques that will be recognized by thoseskilled in the art. The peak or RMS value of the signal received may becalculated using appropriate gain factors to account for the degree ofamplification. The voltage value may then be divided by the senseelectrode spacing to calculate the electric field strength. If thesensor is in the blood, the myocardial field strength may be calculatedby multiplying the blood pool field strength by about 3, to account forthe resistivity differences of blood and the myocardium. This is validunder conditions of uniform current density, and noting the currentcontinuity between the tissue and blood conductors.

In another embodiment, a sensor 18 is a pair of electrodes secured to adeflectable electrophysiology catheter. Sensor 18 electrodes areintroduced into a chamber of the heart. The deflectable catheter may beoriented until a maximum in field strength is measured between theelectrodes. The orientation with maximum field strength occurs when theaxis between the sensor electrodes aligns with the vector of theelectric field. The vector of the electric field is coincident with theaxis between the patch electrodes 14 and 16. The use of a deflectablecatheter facilitates a one-time calibration of field strength as afunction of drive current for a particular patient. The calibration maythen be used in subsequent applications of the therapeutic method to thepatient, without the need for further catheterization.

In yet another embodiment, sensor 18 is a pair of electrodes positionedon a trans-esophageal probe. The sensor electrodes are inserted throughthe esophagus to a position adjacent the patient's heart. Thetrans-esophageal probe is oriented with a first sensor electrodeanterior, or facing the chest of the patient, and the second sensorelectrode posterior, or facing the patient's back. The probe may bepositioned in the cardiac region to make a field measurement, and assuch obviates the need for more invasive catheterization.

In use, sensors 18 may be used to initially measure the field strength,to continually measure the field strength or to periodically measure thefield strength for a particular patient. For example, the field strengthmay be established using an independent sensing apparatus in a clinicalsetting. To establish the threshold, the applied current may beincrementally changed to determine the depolarization threshold for aparticular patient's heart. This type of ‘threshold testing’ may emulateamplitude step-up and step-down protocols as will be recognized by thoseskilled in the art. The cardiac sensing will indicate ectopic oruntoward stimulation. The identification of the ectopic or untowardstimulation will allow the therapeutic current amplitude and frequencyto be set below stimulation threshold with sufficient safety margin.Furthermore, the resultant threshold field strength may be assessed.Continuous or periodic monitoring of the field strength after theinitial therapeutic current level has been set will allow controller 20to adjust the value during therapy. For example, if electrodes 14 and 16are repositioned, the current density through the heart may changesignificantly, if the applied current remained constant. In anunmonitored situation, this could either pose a stimulation danger, orresult in reduced therapy, but with the benefit of this invention, theapplied current may be adjusted dynamically.

The present invention has been described in considerable detail in orderto comply with the patent statutes and to provide those skilled in theart with the information needed to apply the novel principles and toconstruct and use such components to practice the invention. However,upon review of this disclosure, those skilled in the art will recognizethat the invention can be practiced with specifically differentequipment and devices, and that various modifications, both to theapparatus and method, can be accomplished without departing from thescope of the present invention.

1. A method for providing cardiac therapy, comprising: applying astimulus to a heart, the heart positioned between a first electrode anda second electrode; measuring the field strength generated by applyingthe stimulus; and adjusting at least one parameter of the stimulus tomaintain the stimulus below a depolarization threshold of the heartbased on the measuring.
 2. A method, as in claim 1, further comprising:sensing a cardiac cycle of a heart to determine a refractory period ofthe heart; and applying the stimulus to the heart during the refractoryperiod.
 3. A method, as in claim 2, further comprising adjusting atleast one parameter of the stimulus to the heart based on the cardiaccycle.
 4. A method, as in claim 3, wherein the stimulus is continuouslyapplied throughout the cardiac cycle.
 5. A method, as in claim 1,wherein measuring the field strength comprises: inserting the sensorthrough an esophagus to a position adjacent the heart; and orienting thesensor to sense a maximum field strength.
 6. A method, as in claim 1,wherein measuring the field strength comprises: inserting the sensorinto the heart; and orienting the sensor to sense a maximum fieldstrength.